Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 40 year-old woman with acute myelogenous leukemia developed an advanced atrioventricular block and pericardial effusion. On autopsy, pericardial effusion without pericarditis and mononuclear cell infiltration in His bundle were found. Focal infiltration of His bundle by leukemic cells was suggested as the cause of the atrioventricular block.
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PMID:A case of acute myelogenous leukemia with advanced atrioventricular block and pericardial effusion caused by leukemic cell infiltration. 695 55

This study reports on a patient with acute myelogenous leukemia (AML) in remission who had a series of 11 granulocytic sarcomas (chloromas or myeloblastomas) appearing periodically over a 29-month interval in a variety of anatomic sites without evidence of bone marrow recurrence. This isolated extramedullary recurrence of AML is distinctly unusual with only 24 cases described previously. This patient had the greatest number and longest reported interval of recurrent granulocytic sarcomas (GS) before bone marrow relapse. Furthermore, he represents the first case of a patient with GS presenting with both an 8;21 chromosomal translocation and neural cell adhesion molecule (CD56) expression. The authors hypothesize that these two abnormalities identified previously as predisposing factors to GS may, in fact, be synergistic for this phenomenon. His case and the review of the literature demonstrate some of the important clinical and management features of a patient who develops GS while in complete marrow remission from previous AML. Although highly sensitive to radiation therapy, the onset of granulocytic sarcomas is almost always followed by bone marrow relapse and should be treated with aggressive reinduction chemotherapy and local irradiation. Such therapy is associated with the longest interval of disease-free survival.
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PMID:Recurrent granulocytic sarcoma. An unusual variation of acute myelogenous leukemia associated with 8;21 chromosomal translocation and blast expression of the neural cell adhesion molecule. 751 42

We report the in vitro suppression of the IL-3-dependent MO-7 acute myeloid leukemia proliferation by an interleukin-3 antagonist. The antagonist was generated by alkylation to inactivate catalytic His-residues of native human interleukin-3. The resulting inhibitor caused a factor 7 inhibition of the growth-response curve of the IL-3 control-stimulated proliferation of a MO-7 leukemia cell line. A 40% inhibition of the MO-7 proliferation could be achieved with a partially alkylated inhibitor in presence of a factor 30 excess of native IL-3. Therefore, the inhibitor had a substantially improved affinity for the IL-3 receptor on these leukemia cells. At a concentration of as low as 0.1 ng/ml it still caused a 2-fold inhibition of the native IL-3-stimulated proliferation response curve. Thus it can be concluded that this alkylate IL-3 is a potent IL-3 antagonist. Based on the reported specific zinc binding of IL-2, IL-6, GM-CSF and gamma-interferon this suggests that more leukemias and even other forms of cancer can be effectively suppressed by alkylated growth factors.
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PMID:In vitro suppression of leukemia by alkylated interleukin-3. 776 58

Patients who have received cytotoxic therapy for primary neoplastic disease are at an increased risk of developing secondary (therapy-related) acute myeloid leukaemia (AML) or myelodysplasia (MDS). RAS and FMS mutations have been observed in patients with AML and MDS. It has been suggested that the mutational status within these genes may be predictive of early secondary leukaemic disease. In this study we have screened 50 haematologically normal patients in complete remission from childhood acute lymphoblastic leukaemia (ALL) for activating point mutations in the RAS and FMS proto-oncogenes. Such patients may be considered at risk of therapy-related disease. Codons 12, 13 and 61 were screened in RAS and codon 969 in FMS using the polymerase chain reaction (PCR) followed by oligonucleotide hybridization (ONH). Three of the 50 patients (6%) were found to harbour N12 RAS mutations. One of these three patients (2%) had both a N12 RAS and FMS 969 mutation. Upon sequencing the RAS mutations, substitutions of serine, cysteine and aspartic acid for glycine were identified. The FMS 969 mutation was also confirmed, by sequencing, as a histidine substitution. RAS mutations were not detected in presentation samples indicating that these lesions have been somatically acquired presumably subsequent to cytotoxic therapy for the primary disease. Continued follow-up of these patients may indicate a role for these mutations in the development of secondary malignancies.
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PMID:RAS and FMS mutations following cytotoxic therapy for childhood acute lymphoblastic leukaemia. 756 28

A case of Sweet syndrome (SS) associated with acute megakaryoblastic leukemia (AMKL) is reported. A 66-year-old male was admitted to Ashikaga Red Cross Hospital because of skin eruption and sore throat. His eruption was tender and erythema-like nature. He developed a spiking fever after admission. CBC revealed pancytopenia, and a bone marrow specimen showed increased megakaryoblasts and fibrosis. These blasts were shown to be CD41-positive by flow cytometric analysis. A diagnosis of AMKL was then made. Skin biopsy revealed infiltration of neutrophils without vasculitis, compatible with SS. Oral administration of prednisolone was begun which improved his skin lesions considerably. He was then treated with low dose Ara-C, which was however ineffective. The blasts increased in the peripheral blood and he died on the 72nd hospital day. There are 37 reported cases of SS associated with acute nonlymphocytic leukemia, and this is the first case report of SS associated with AMKL.
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PMID:[Acute megakaryoblastic leukemia associated with Sweet's syndrome, including review of the literature]. 847 86

A 64-year-old man who had been diagnosed as having acute myelocytic leukemia (M2 in the FAB classification) developed central nervous system involvement of intramedullary spinal cord during hematological remission. Magnetic resonance imaging showed a low signal intensity mass on T1-weighted images and a high signal intensity mass on T2-weighted images. The mass was slightly enhanced by gadolinium-diethylenetriaminepentaacetic acid. His neurological symptoms were slightly improved by intrathecal and systemic chemotherapy combined with external irradiation, although the size of the mass did not change.
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PMID:Acute myelocytic leukemia relapse with intramedullary spinal cord tumor involvement during hematological remission. 858 May 60

A 54-year-old male was admitted because of dyspnea on exercise. His peripheral blood revealed pancytopenia with severely hypoplastic bone marrow. Bone marrow aspiration showed a marked hypocellular marrow with 62.4% of blast cells. Cytochemical studies showed that peroxidase activity, alpha-nephtyl buthylate esterase activity and PAS reaction were negative, and that only ASD-chroloacetate esterase activity was positive. Surface marker analysis of blast cells showed positive result for CD5, 7, 33 and 34 antigens. The T-cell receptor beta gene was rearranged, but the immunoglobulin H chain gene showed a germ line configuration. Terminal Deoxynucleotydyl Transferase (TdT) was positive, but cellular surface and cytoplasmic immunoglobulin were not recognized. A diagnosis of hypoplastic mixed lineage leukemia was made and treated with low dose cytosine arabinoside, he resulted in complete remission. The relation between hypoplastic leukemia, AML-M0 and mixed lineage leukemia was also discussed.
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PMID:[Hypoplastic mixed lineage leukemia successfully treated with low-dose cytosine arabinoside]. 872 48

We present the case of a 67-year-old male with primary extramedullary leukemia of the prostate gland, the first reported case in the literature to the best of our knowledge. His initial symptoms consisted of episodes of urinary retention. He underwent transurethral resection of the prostate, and a diagnosis of high-grade lymphoma was rendered. He then received a course of doxorubicin-based lymphoma chemotherapy regimen. However, based on a panel of immunocytochemical stains, a diagnosis of extramedullary leukemia or chloroma was confirmed. His bone-marrow examination at this point was normal. He underwent radiation therapy to the prostate with a total dose of 3960 cGy. Seven months after his initial presentation, he progressed to acute nonlymphocytic leukemia (ANLL), M2 by FAB classification. He was successfully treated with induction and consolidation chemotherapy with Ara-C and idarubicin, and was maintained in complete remission up to 19 months of follow-up. Eight other cases of prostatic leukemia reported in the literature are presented. Five cases occurred in association with ANLL, 2 cases as sites of ANLL relapse, and 1 case in association with myelodysplasia. The use of immunohistochemical stains has aided us in diagnosis of extramedullary leukemia. Surgery, radiation therapy, and chemotherapy play complementary roles in the treatment of prostatic extramedullary leukemia.
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PMID:Primary extramedullary leukemia of the prostate: case report and review of the literature. 894 69

The t(7;11)(p15;p15) translocation is an uncommon balanced aberration which has been found predominantly in Orientals, frequently presenting as de novo acute myeloid leukemia (AML) and occasionally as chronic myeloid leukemia in blastic crisis. This paper reports the first case of therapy-related AML (t-AML) with t(7;11). The patient was a 36-year-old Chinese man with a longstanding psoriasis for which he had received bimolane and ICRF-154 therapy. His cytology and cytochemistry were compatible with M2 subtype of AML. He achieved a complete remission after two courses of HA regimen (homoharringtonine and Ara-c). Six months later, he relapsed and died of overwhelming infection after 3 months. Chromosome analysis on bone marrow cells using short-term culture and R-banding at presentation revealed his karyotype to be 46,XY,t(7;11)(p15;p15)/ 46,XY,t(7;11)(p15;p15),del(12)(p12)/ 46,XY. This case implies: (1) dioxopiperazine derivatives can induce AML with t(7;11) in addition to inducing AML with t(15;17) or t(8;21); (2) t(7;11) may be found not only in de novo AML, but also in t-AML. Chromosomal translocation t(7;11) should be added to t(8;21), t(15;17) and inv(16) as favourable cytogenetic abnormalities associated with t-AML.
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PMID:Translocation t(7;11)(P15;P15) in a patient with therapy-related acute myeloid leukemia following bimolane and ICRF-154 treatment for psoriasis. 911 26

A case of acute myeloid leukaemia presenting as pyrexia of unknown origin and weight loss with pancytopenia is described. Initial investigations revealed trilineage myelodysplasia which evolved into acute myeloid leukaemia within 2 weeks of presentation. He was commenced on a standard induction regimen consisting of idarubicin, Ara-C and thioguanine. Throughout his hospital stay he remained febrile. In spite of exhaustive investigations no cause for the pyrexia was found nor did he respond to any form of treatment. He died after 9 weeks in hospital. His post-mortem examination revealed widespread disseminated tuberculosis without any reactive inflammatory tissue response or granuloma formation.
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PMID:Acute myeloid leukaemia complicated by anergic tuberculosis. 911 7


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